Biology subjects

Voronina, E.

Publications and source records attributed to Voronina, E..

4 recordsLinked to original sources

bioRxiv2026

An axiomatic approach to cultivar ranking in multi-environment trials

AO_SCPLOWBSTRACTC_SCPLOWMulti-environment trials are central to cultivar evaluation because they reveal how candidate cultivars perform across locations, years, management conditions, and stress environments. The resulting yield matrix is a rich source of data on genotype-by-environment interaction, and a wide literature on estimation, decomposition, visualisation, and prediction of yield potential and stability has flourished. However the ultimate question of which cultivar to recommend on the basis of such a matrix is often left implicit. The question is far from trivial, and in this paper we formulate cultivar recommendation as an axiomatic ranking problem. This framework is rich enough to encompass the existing literature on stability indices, as well as any other deterministic ranking procedure. We show that many commonly used stability-based procedures can violate minimal criteria of efficiency or consistency. The result of such violations is that a cultivar with uniformly high yield could be ranked below a cultivar with uniformly low yield, or the relative ranks of two cultivars could depend on whether or not a third cultivar is present in the matrix. Our results prove that under a small number of such criteria the space of admissible rules collapses to the family of power means and their limiting cases. If we further wish to allow multiplication normalisation of yield, we are left with the geometric mean as the unique solution.

genetics↗

bioRxiv2022

Tripartite interactions between filamentous Pf4 bacteriophage, Pseudomonas aeruginosa, and bacterivorous nematodes

The opportunistic pathogen Pseudomonas aeruginosa PAO1 is infected by the filamentous bacteriophage Pf4. Pf4 virions promote biofilm formation, protect bacteria from antibiotics, and modulate animal immune responses in ways that promote infection. Furthermore, strains cured of their Pf4 infection ({Delta}Pf4) are less virulent in animal models of infection. Consistently, we find that strain {Delta}Pf4 is less virulent in a Caenorhabditis elegans nematode infection model. However, our data indicate that PQS quorum sensing is activated and production of the pigment pyocyanin, a potent virulence factor, is enhanced in strain {Delta}Pf4. The reduced virulence of {Delta}Pf4 despite high levels of pyocyanin production may be explained by our finding that C. elegans mutants unable to sense bacterial pigments through the aryl hydrocarbon receptor are more susceptible to {Delta}Pf4 infection compared to wild-type C. elegans. Collectively, our data support a model where suppression of quorum-regulated virulence factors by Pf4 allows P. aeruginosa to evade detection by innate host immune responses. Author SummaryPseudomonas aeruginosa is an opportunistic bacterial pathogen that infects wounds, lungs, and medical hardware. P. aeruginosa strains are often themselves infected by a filamentous virus (phage) called Pf. At sites of infection, filamentous Pf virions are produced that promote bacterial colonization and virulence. Here, we report that strains of P. aeruginosa cured of their Pf infection are less virulent in a Caenorhabditis elegans nematode infection model. We also report that PQS quorum sensing and production of the virulence factor pyocyanin are enhanced in P. aeruginosa strains cured of their Pf infection. Compared to wild-type C. elegans, nematodes unable to detect bacterial pigments via the aryl hydrocarbon receptor AhR were more susceptible to infection by Pf-free P. aeruginosa strains that over-produce pyocyanin. Collectively, this study supports a model where Pf phage suppress P. aeruginosa PQS quorum sensing and reduce pyocyanin production, allowing P. aeruginosa to evade AhR-mediated immune responses in C. elegans.

microbiology↗

bioRxiv2022

COP9 signalosome component CSN-5 stabilizes PUF proteins FBF-1 and FBF-2 in C. elegans germline stem cells

RNA-binding proteins FBF-1 and FBF-2 (FBFs) are required for germline stem cell maintenance and the sperm/oocyte switch in Caenorhabditis elegans, though the mechanisms controlling FBF protein levels remain unknown. We identified an interaction between both FBFs and CSN-5, a component of the COP9 (constitutive photomorphogenesis 9) signalosome. Here, we find that the MPN (Mpr1/Pad1 N terminal) metalloprotease domain of CSN-5 interacts with the PUF (Pumilio and FBF) RNA-binding domain of FBFs and the interaction is conserved for human homologs PUM1 and CSN5. The interaction between FBF-2 and CSN-5 can be detected in vivo by proximity ligation. csn-5 mutation results in destabilization of FBF proteins, a decrease in the numbers of germline stem cells, and disruption of the switch from spermatogenesis to oogenesis. The loss of csn-5 does not decrease the levels of a related PUF protein PUF-3 and csn-5(lf) phenotype is not enhanced by fbf-1/2 depletion, suggesting that the effect is specific to FBFs. The effect of csn-5 on germline sex determination is largely independent of the COP9 signalosome and is cell autonomous. Surprisingly, regulation of FBF protein levels involves a combination of COP9-dependent and -independent mechanisms differentially affecting FBF-1 and FBF-2. This work supports a previously unappreciated role for CSN-5 in stabilization of germline stem cell regulatory proteins FBF-1 and FBF-2. Author SummaryGerm cell development and reproductive success in the nematode C. elegans rely on the function of germline stem cells. Continued maintenance of these cells is supported by the activity of conserved RNA-binding proteins FBF-1 and FBF-2 (FBFs). However, it is unknown how FBF protein levels are regulated. Here, we identify a direct interaction between FBFs and CSN-5, a component of the COP9 signalosome best known for its role in regulating protein degradation. We find that CSN-5 promotes FBF stability and allows for accumulation of steady-state protein levels, thereby promoting FBF function. In csn-5 mutants, we find a significant reduction of FBF proteins, decrease of stem cells, and failure to promote oogenesis consistent with compromised FBF function. Furthermore, CSN-5 contributes to FBF protein stability through two mechanisms. This work demonstrates a previously unappreciated role for CSN-5 in stabilization of FBF proteins. Based on our finding that the FBF/CSN-5 interaction is conserved and detectable between homologous human proteins, we speculate this relationship might be relevant for understanding stem cell maintenance in a range of species, from nematodes to humans.

developmental biology↗

bioRxiv2019

PUF family proteins FBF-1 and FBF-2 regulate germline stem and progenitor cell proliferation and differentiation in C. elegans

Stem cells support tissue maintenance, but the mechanisms that balance the rate of stem cell self-renewal with differentiation at a population level remain uncharacterized. Through investigating the regulation of germline stem cells by two PUF family RNA-binding proteins FBF-1 and FBF-2 in C. elegans, we find that FBF-1 restricts differentiation, while FBF-2 promotes both proliferation and differentiation. FBFs act on a shared set of target mRNAs; however, FBF-1 destabilizes target transcripts, while FBF-2 promotes their accumulation. These regulatory differences result in complementary effects of FBFs on stem cells. We identify a mitotic cyclin as one of the targets affecting stem cell homeostasis. FBF-1-mediated translational control requires the activity of CCR4-NOT deadenylase. Distinct abilities of FBFs to cooperate with CCR4-NOT depend on protein sequences outside of the conserved PUF family RNA-binding domain. We propose that the combination of FBF activities regulates the dynamics of germline stem cell proliferation and differentiation.

developmental biology↗